Prdx1 Inhibits Tumorigenesis via Regulating PTEN/AKT Activity

DSpace/Manakin Repository

Prdx1 Inhibits Tumorigenesis via Regulating PTEN/AKT Activity

Citable link to this page

. . . . . .

Title: Prdx1 Inhibits Tumorigenesis via Regulating PTEN/AKT Activity
Author: Cao, Juxiang; Schulte, Jennifer; Knight, Alexander; Leslie, Nicholas R; Zagozdzon, Agnieszka; Manevich, Yefim; Beeson, Craig; Neumann, Carola A; Bronson, Roderick Terry

Note: Order does not necessarily reflect citation order of authors.

Citation: Cao, Juxiang, Jennifer Schulte, Alexander Knight, Nicholas R. Leslie, Agnieszka Zagozdzon, Roderick Bronson, Yefim Manevich, Craig Beeson, and Carola A. Neumann. 2009. Prdx1 inhibits tumorigenesis via regulating PTEN/AKT activity. EMBO Journal 28(10): 1505-1517.
Full Text & Related Files:
Abstract: It is widely accepted that reactive oxygen species (ROS) promote tumorigenesis. However, the exact mechanisms are still unclear. As mice lacking the peroxidase peroxiredoxin1 (Prdx1) produce more cellular ROS and die prematurely of cancer, they offer an ideal model system to study ROS-induced tumorigenesis. Prdx1 ablation increased the susceptibility to Ras-induced breast cancer. We, therefore, investigated the role of Prdx1 in regulating oncogenic Ras effector pathways. We found Akt hyperactive in fibroblasts and mammary epithelial cells lacking Prdx1. Investigating the nature of such elevated Akt activation established a novel role for Prdx1 as a safeguard for the lipid phosphatase activity of PTEN, which is essential for its tumour suppressive function. We found binding of the peroxidase Prdx1 to PTEN essential for protecting PTEN from oxidation-induced inactivation. Along those lines, Prdx1 tumour suppression of Ras- or ErbB-2-induced transformation was mediated mainly via PTEN.
Published Version: doi:10.1038/emboj.2009.101
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2688529/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:5011927

Show full Dublin Core record

This item appears in the following Collection(s)

 
 

Search DASH


Advanced Search
 
 

Submitters